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Molecular Mechanisms Underlying Metastatic Potential in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 1184

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Guest Editor
SSD-Innovative Therapies for Abdominal Metastases, Department of Abdominal Oncology, Istituto Nazionale Tumori di Napoli IRCCS “G. Pascale”, via M. Semmola, 80131 Naples, Italy
Interests: cancer genetics; gastro-intestinal oncology; oligo-metastatic disease; molecular oncology; precision oncology
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Guest Editor
Pathology Unit, Istituto Nazionale Tumori, IRCCS Fondazione “G. Pascale”, 80131 Napoli, Italy
Interests: histology; molecular biology; pathology; cancer biomarkers; cancer metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer metastasis is the leading cause of cancer-related mortality, representing a complex cascade of events that enable cancer cells to disseminate from the primary tumor, survive in transit, and colonize distant organs. Understanding the molecular underpinnings that drive metastasis is crucial for developing targeted therapies that can effectively hinder this lethal process.

Deep scientific exploration of certain areas can be fundamental to understanding the phenomenon of metastasis. Specifically, defining the genetic regulators of metastasis can be achieved through the identification and characterization of genes and epigenetic alterations that enhance metastatic potential and/or drive organotropism. This includes the role of specific oncogenes, tumor suppressor genes, DNA epigenetic modifications, and non-coding RNAs. Furthermore, direct evidence of the molecular partners involved in metastasis can come from proteomic insights into metastatic progression. In this context, proteomic profiles associated with metastatic versus non-metastatic cancer cells can elucidate the functional roles of specific proteins in cell migration, invasion, and colonization. Post-translational modifications and their impact on metastatic behavior is another field that warrants in-depth investigation. Finally, the identification of signaling pathways involved in the metastatic cascade (including epithelial–mesenchymal transition, angiogenesis, immune evasion, etc.) can be crucial. All the phenomena and potential areas of interest described can lead to the discovery of novel therapeutic targets impacting metastatic behavior.

Leading by Prof. Dr. Alessandro Ottaiano and Dr. Annabella Di Mauro, assisting by our Topical Advisory Panel Member Dr. Mariachiara Santorsola(Istituto Nazionale Tumori IRCCS–Fondazione G Pascale), this Special Issue invites original research articles, reviews, and perspectives addressing molecular factors influencing tumor metastasis. Articles consisting exclusively of bioinformatics or computational analyses of public databases or pure clinical studies will not be accepted. Predictive models of metastatic progression based on molecular data from real-world patients are welcome.

 

Prof. Dr. Alessandro Ottaiano

Dr. Annabella Di Mauro
Guest Editors

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Keywords

  • cancer metastasis
  • cancer virulence
  • oncogenes
  • epithelial-mesenchymal transition
  • angiogenesis
  • cancer genetics

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Published Papers (1 paper)

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8 pages, 1354 KiB  
Case Report
Autoimmune Pancreatitis Mimicking a Pancreatic Neuroendocrine Tumor: A Case Report with a Literature Review
by Marianna Franchina, Liliana Dell’Oro and Sara Massironi
Int. J. Mol. Sci. 2025, 26(4), 1536; https://doi.org/10.3390/ijms26041536 - 12 Feb 2025
Viewed by 893
Abstract
Autoimmune pancreatitis (AIP) is a rare chronic pancreatitis subtype that often mimics pancreatic cancer due to the overlapping clinical and radiological features, posing significant diagnostic challenges. Similarly, distinguishing AIP from pancreatic neuroendocrine neoplasms (PanNENs), which present with nonspecific symptoms, adds complexity to clinical [...] Read more.
Autoimmune pancreatitis (AIP) is a rare chronic pancreatitis subtype that often mimics pancreatic cancer due to the overlapping clinical and radiological features, posing significant diagnostic challenges. Similarly, distinguishing AIP from pancreatic neuroendocrine neoplasms (PanNENs), which present with nonspecific symptoms, adds complexity to clinical evaluations. We present the case of a 46-year-old male with recurrent acute idiopathic pancreatitis. Abdominal computed tomography (CT) revealed a 25 mm hypodense mass in the pancreatic tail with mild arterial contrast enhancement. Magnetic resonance imaging (MRI) showed the mass to be hypointense on T2-weighted sequences, with no diffusion restriction and an enhancement pattern akin to normal pancreatic tissue. The endoscopic ultrasound-guided fine needle biopsy (EUS-FNB) was inconclusive. Gallium-68 DOTATATE positron emission tomography–CT (Ga-68 DOTATATE PET-CT) showed an increased tracer uptake, leading to a distal pancreatectomy with a splenectomy. Histopathology demonstrated chronic sclerotic pancreatitis with inflammatory infiltrates. Elevated serum IgG4 levels confirmed the diagnosis of type 1 AIP Differentiating AIP from pancreatic malignancies, including PanNENs, is both critical and complex. This case highlights a misdiagnosis of PanNENs in a patient with focal AIP, where neuroendocrine hyperplasia and islet cell clusters within fibrotic areas mimicked PanNENs, even on Ga-68 PET-CT. The findings emphasize the potential for false positives with Ga-68 DOTATATE PET-CT and the importance of integrating clinical, radiological, and histological data for an accurate diagnosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Metastatic Potential in Cancer)
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